Iron-overloaded follicular fluid increases the risk of endometriosis-related infertility by triggering granulosa cell ferroptosis and oocyte dysmaturity

Chen

et al. 2023

Preprint

Ferroptosis, a cohering network integrating iron, amino acids, lipids, and redox chemicals together，is a unique regulated cell death (RCD). Iron overload, excessive reactive oxygen species (ROS), and lipid peroxidation all contribute to the onset of ferroptosis. In recent years, a growing body of evidence suggests that ferroptosis is associated with some female reproductive diseases. The purpose of our review is to give a brief description of ferroptosis activation mechanism and relationship to female reproductive diseases including infertility, pregnancy associated diseases and ovarian cancer.

Section: The Two Sides Effects Of Ferroptosis In Emsmentioning

confidence: 99%

Ferroptosis in female reproductive diseases: from potential pathogenesis to therapy

Chen

et al. 2023

Preprint

“…This effect requires MUFA activation by acyl-coenzyme A synthetase long-chain family member 3 (ACSL3) and is independent of lipid droplet formation ( 68 ). In addition, lipid peroxidation is inhibited by Fer-1, liproxstatin-1 (Lip-1), and vitamin E, which are free radical scavengers that reduce lipid peroxidation and effectively block ferroptosis ( 69 , 70 ). Ferroptosis suppressor protein 1 (FSP1) suppresses ferroptosis independent of GSH.…”

Section: Antioxidant Systemsmentioning

confidence: 99%

Ferroptosis and musculoskeletal diseases: “Iron Maiden” cell death may be a promising therapeutic target

Huang

et al. 2022

Front. Immunol.

Ferroptosis is a novel form of cell death precisely regulated by iron metabolism, antioxidant processes, and lipid metabolism that plays an irreplaceable role in the development of many diseases. Musculoskeletal disorders (MSKs), including osteoporosis, osteoarthritis, rheumatoid arthritis, intervertebral disc degeneration, sarcopenia, and rhabdomyolysis, have become one of the most common causes of disability and a major burden on public health and social care systems. The mechanism of ferroptosis in MSKs has recently been elucidated. In this review, we briefly introduce the ferroptosis mechanism and illustrate the pathological roles of ferroptosis in MSKs with a focus on how ferroptosis can be exploited as a promising treatment strategy. Notably, because the toxicity of compounds that inhibit or induce ferroptosis in other organs is largely unknown, ferroptosis appears to be a double-edged sword. We point out that more research is needed in the future to verify the therapeutic effects based on ferroptosis in MSKs.

“…Iron (Fe) homeostasis, including the involvement of specific proteins [ 15 , 16 , 17 , 18 , 19 , 20 , 21 ], is directly related to the pathophysiology of endometriosis. In the course of endometriosis there is a correlation between the release of iron from erythrocytes, apoptotic endometrial tissue and cell debris which sweep into the peritoneal cavity and create a pro-inflammatory and pro-oxidative environment [ 22 , 23 , 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

“…Its excessive accumulation in cells, tissues and organs is toxic and leads to various diseases [ 22 ]. Iron overload caused by retrograde menstruation and periodic hemorrhage from ectopic lesions in the peritoneal fluid is an important factor promoting the inflammatory microenvironment [ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

The Influence of Lactoferrin in Plasma and Peritoneal Fluid on Iron Metabolism in Women with Endometriosis

Skarżyńska

Wróbel

Zborowska

et al. 2023

IJMS

The aim of this study was to investigate the relationship between lactoferrin and iron and its binding proteins in women with endometriosis by simultaneously measuring these parameters in plasma and peritoneal fluid. Ninety women were evaluated, of whom 57 were confirmed as having endometriosis. Lactoferrin was measured by ELISA, transferrin, ferritin and iron on a Cobas 8000 analyser. Lactoferrin and transferrin in peritoneal fluid were lower compared to plasma, in contrast to ferritin and iron. In plasma, lactoferrin showeds associations with iron and transferrin in endometriosis and with ferritin in the group without endometriosis. Lactoferrin in peritoneal fluid correlated with lactoferrin, iron and transferrin of plasma in patients without endometriosis. The ratio of lactoferrin concentration in peritoneal fluid to plasma differentiated stage I versus IV of endometriosis and was negatively correlated with the iron ratio in patients without endometriosis. The ferritin ratio differentiated women with and without endometriosis. The very high ferritin ratios, especially in advanced stages of endometriosis, suggest the protective involvement of this protein in peritoneal fluid and the loss of this role by lactoferrin. The results demonstrate the validity of assessing iron metabolism in women with endometriosis, which may be useful as a marker of the disease and its progression.